Small MAF genes variants and chronic myeloid leukemia

Chronic myeloid leukemia (CML) is one of the most frequent hematological neoplasia worldwide. The abnormal accumulation of reactive oxygen species may be an important factor in CML development. The transcription factor NRF2 can regulate the transcription of a battery of antioxidant and detoxificant...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:European journal of haematology 2014-01, Vol.92 (1), p.35-41
Hauptverfasser: Martínez-Hernández, Angelica, Gutierrez-Malacatt, Humberto, Carrillo-Sánchez, Karol, Saldaña-Alvarez, Yolanda, Rojas-Ochoa, Alberto, Crespo-Solis, Erick, Aguayo-González, Alvaro, Rosas-López, Adriana, Ayala-Sanchez, Jose Manuel, Aquino-Ortega, Xochitl, Orozco, Lorena, Cordova, Emilio J
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 41
container_issue 1
container_start_page 35
container_title European journal of haematology
container_volume 92
creator Martínez-Hernández, Angelica
Gutierrez-Malacatt, Humberto
Carrillo-Sánchez, Karol
Saldaña-Alvarez, Yolanda
Rojas-Ochoa, Alberto
Crespo-Solis, Erick
Aguayo-González, Alvaro
Rosas-López, Adriana
Ayala-Sanchez, Jose Manuel
Aquino-Ortega, Xochitl
Orozco, Lorena
Cordova, Emilio J
description Chronic myeloid leukemia (CML) is one of the most frequent hematological neoplasia worldwide. The abnormal accumulation of reactive oxygen species may be an important factor in CML development. The transcription factor NRF2 can regulate the transcription of a battery of antioxidant and detoxificant genes after heterodimerizing with small‐Maf proteins. Although the participation of NRF2 in the development of chronic degenerative diseases has been thoroughly studied, the role of small‐Maf genes has not been documented. We have identified polymorphisms in the three MAF genes (F, G and K) and assessed their association with CML. Over 266 subjects with CML and 399 unrelated healthy donors have been studied. After sequencing each MAF gene by Sanger technology, we found 17 variants in MAFF gene, eight in MAFG and seven in MAFK. In the case‐control study, the homozygote genotype CC for the rs9610915 SNP of MAFF was significantly associated with CML. The frequency of the ACC haplotype from MAFK was significantly lower than controls. After stratification by gender, the ACC and GTG haplotypes were associated only with males with CML. These novel data suggest an association between MAFF and MAFG and the development of CML.
doi_str_mv 10.1111/ejh.12211
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1534840101</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1534840101</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4621-1ae934c132fb2ea8994094f6b11b042d8a3fe1dae958813ee2e8501c52eb3b0f3</originalsourceid><addsrcrecordid>eNqFkLtOw0AQRVcIBOFR8APIJRQOM7vrx5ZRlAAmgBAgytXaHoMTP4I3BvL3GAx0iGmmOfcUh7FDhCF2d0rz5yFyjrjBBugDuOCD2mQDUMBdKSXusF1r5wDAFQbbbIdLxFB6wYB5d6UpCudqNHWeqCLrvJomN9XKOqZKneS5qas8cco1FXWeOgW1Cypzs8-2MlNYOvj-e-xhOrkfn7uzm7OL8WjmJtLn6KIhJWSCgmcxJxMqJUHJzI8RY5A8DY3ICNOO8sIQBRGn0ANMPE6xiCETe-y49y6b-qUlu9JlbhMqClNR3VqNnpChBAT8H5WKB10BoTr0pEeTpra2oUwvm7w0zVoj6M-guguqv4J27NG3to1LSn_Jn4IdcNoDb3lB679NehKd_yjdfpHbFb3_Lkyz0H4gAk8_Xp_p6FJG00iE-lZ8AM9di6o</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1492700039</pqid></control><display><type>article</type><title>Small MAF genes variants and chronic myeloid leukemia</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Martínez-Hernández, Angelica ; Gutierrez-Malacatt, Humberto ; Carrillo-Sánchez, Karol ; Saldaña-Alvarez, Yolanda ; Rojas-Ochoa, Alberto ; Crespo-Solis, Erick ; Aguayo-González, Alvaro ; Rosas-López, Adriana ; Ayala-Sanchez, Jose Manuel ; Aquino-Ortega, Xochitl ; Orozco, Lorena ; Cordova, Emilio J</creator><creatorcontrib>Martínez-Hernández, Angelica ; Gutierrez-Malacatt, Humberto ; Carrillo-Sánchez, Karol ; Saldaña-Alvarez, Yolanda ; Rojas-Ochoa, Alberto ; Crespo-Solis, Erick ; Aguayo-González, Alvaro ; Rosas-López, Adriana ; Ayala-Sanchez, Jose Manuel ; Aquino-Ortega, Xochitl ; Orozco, Lorena ; Cordova, Emilio J</creatorcontrib><description>Chronic myeloid leukemia (CML) is one of the most frequent hematological neoplasia worldwide. The abnormal accumulation of reactive oxygen species may be an important factor in CML development. The transcription factor NRF2 can regulate the transcription of a battery of antioxidant and detoxificant genes after heterodimerizing with small‐Maf proteins. Although the participation of NRF2 in the development of chronic degenerative diseases has been thoroughly studied, the role of small‐Maf genes has not been documented. We have identified polymorphisms in the three MAF genes (F, G and K) and assessed their association with CML. Over 266 subjects with CML and 399 unrelated healthy donors have been studied. After sequencing each MAF gene by Sanger technology, we found 17 variants in MAFF gene, eight in MAFG and seven in MAFK. In the case‐control study, the homozygote genotype CC for the rs9610915 SNP of MAFF was significantly associated with CML. The frequency of the ACC haplotype from MAFK was significantly lower than controls. After stratification by gender, the ACC and GTG haplotypes were associated only with males with CML. These novel data suggest an association between MAFF and MAFG and the development of CML.</description><identifier>ISSN: 0902-4441</identifier><identifier>EISSN: 1600-0609</identifier><identifier>DOI: 10.1111/ejh.12211</identifier><identifier>PMID: 24118457</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Adult ; Alleles ; Case-Control Studies ; Computational Biology ; Female ; Gene Frequency ; Genetic Variation ; Genotype ; Haplotypes ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics ; MafF Transcription Factor - genetics ; MAFG ; MAFK ; MafK Transcription Factor - genetics ; Male ; Middle Aged ; Nuclear Proteins - genetics ; Odds Ratio ; oxidative stress ; Polymorphism, Single Nucleotide ; polymorphisms ; Proto-Oncogene Proteins c-maf - genetics ; re-sequencing ; Sex Factors</subject><ispartof>European journal of haematology, 2014-01, Vol.92 (1), p.35-41</ispartof><rights>2013 John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons Ltd</rights><rights>2013 John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4621-1ae934c132fb2ea8994094f6b11b042d8a3fe1dae958813ee2e8501c52eb3b0f3</citedby><cites>FETCH-LOGICAL-c4621-1ae934c132fb2ea8994094f6b11b042d8a3fe1dae958813ee2e8501c52eb3b0f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fejh.12211$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fejh.12211$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24118457$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martínez-Hernández, Angelica</creatorcontrib><creatorcontrib>Gutierrez-Malacatt, Humberto</creatorcontrib><creatorcontrib>Carrillo-Sánchez, Karol</creatorcontrib><creatorcontrib>Saldaña-Alvarez, Yolanda</creatorcontrib><creatorcontrib>Rojas-Ochoa, Alberto</creatorcontrib><creatorcontrib>Crespo-Solis, Erick</creatorcontrib><creatorcontrib>Aguayo-González, Alvaro</creatorcontrib><creatorcontrib>Rosas-López, Adriana</creatorcontrib><creatorcontrib>Ayala-Sanchez, Jose Manuel</creatorcontrib><creatorcontrib>Aquino-Ortega, Xochitl</creatorcontrib><creatorcontrib>Orozco, Lorena</creatorcontrib><creatorcontrib>Cordova, Emilio J</creatorcontrib><title>Small MAF genes variants and chronic myeloid leukemia</title><title>European journal of haematology</title><addtitle>Eur J Haematol</addtitle><description>Chronic myeloid leukemia (CML) is one of the most frequent hematological neoplasia worldwide. The abnormal accumulation of reactive oxygen species may be an important factor in CML development. The transcription factor NRF2 can regulate the transcription of a battery of antioxidant and detoxificant genes after heterodimerizing with small‐Maf proteins. Although the participation of NRF2 in the development of chronic degenerative diseases has been thoroughly studied, the role of small‐Maf genes has not been documented. We have identified polymorphisms in the three MAF genes (F, G and K) and assessed their association with CML. Over 266 subjects with CML and 399 unrelated healthy donors have been studied. After sequencing each MAF gene by Sanger technology, we found 17 variants in MAFF gene, eight in MAFG and seven in MAFK. In the case‐control study, the homozygote genotype CC for the rs9610915 SNP of MAFF was significantly associated with CML. The frequency of the ACC haplotype from MAFK was significantly lower than controls. After stratification by gender, the ACC and GTG haplotypes were associated only with males with CML. These novel data suggest an association between MAFF and MAFG and the development of CML.</description><subject>Adult</subject><subject>Alleles</subject><subject>Case-Control Studies</subject><subject>Computational Biology</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genetic Variation</subject><subject>Genotype</subject><subject>Haplotypes</subject><subject>Humans</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</subject><subject>MafF Transcription Factor - genetics</subject><subject>MAFG</subject><subject>MAFK</subject><subject>MafK Transcription Factor - genetics</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Nuclear Proteins - genetics</subject><subject>Odds Ratio</subject><subject>oxidative stress</subject><subject>Polymorphism, Single Nucleotide</subject><subject>polymorphisms</subject><subject>Proto-Oncogene Proteins c-maf - genetics</subject><subject>re-sequencing</subject><subject>Sex Factors</subject><issn>0902-4441</issn><issn>1600-0609</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkLtOw0AQRVcIBOFR8APIJRQOM7vrx5ZRlAAmgBAgytXaHoMTP4I3BvL3GAx0iGmmOfcUh7FDhCF2d0rz5yFyjrjBBugDuOCD2mQDUMBdKSXusF1r5wDAFQbbbIdLxFB6wYB5d6UpCudqNHWeqCLrvJomN9XKOqZKneS5qas8cco1FXWeOgW1Cypzs8-2MlNYOvj-e-xhOrkfn7uzm7OL8WjmJtLn6KIhJWSCgmcxJxMqJUHJzI8RY5A8DY3ICNOO8sIQBRGn0ANMPE6xiCETe-y49y6b-qUlu9JlbhMqClNR3VqNnpChBAT8H5WKB10BoTr0pEeTpra2oUwvm7w0zVoj6M-guguqv4J27NG3to1LSn_Jn4IdcNoDb3lB679NehKd_yjdfpHbFb3_Lkyz0H4gAk8_Xp_p6FJG00iE-lZ8AM9di6o</recordid><startdate>201401</startdate><enddate>201401</enddate><creator>Martínez-Hernández, Angelica</creator><creator>Gutierrez-Malacatt, Humberto</creator><creator>Carrillo-Sánchez, Karol</creator><creator>Saldaña-Alvarez, Yolanda</creator><creator>Rojas-Ochoa, Alberto</creator><creator>Crespo-Solis, Erick</creator><creator>Aguayo-González, Alvaro</creator><creator>Rosas-López, Adriana</creator><creator>Ayala-Sanchez, Jose Manuel</creator><creator>Aquino-Ortega, Xochitl</creator><creator>Orozco, Lorena</creator><creator>Cordova, Emilio J</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>201401</creationdate><title>Small MAF genes variants and chronic myeloid leukemia</title><author>Martínez-Hernández, Angelica ; Gutierrez-Malacatt, Humberto ; Carrillo-Sánchez, Karol ; Saldaña-Alvarez, Yolanda ; Rojas-Ochoa, Alberto ; Crespo-Solis, Erick ; Aguayo-González, Alvaro ; Rosas-López, Adriana ; Ayala-Sanchez, Jose Manuel ; Aquino-Ortega, Xochitl ; Orozco, Lorena ; Cordova, Emilio J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4621-1ae934c132fb2ea8994094f6b11b042d8a3fe1dae958813ee2e8501c52eb3b0f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adult</topic><topic>Alleles</topic><topic>Case-Control Studies</topic><topic>Computational Biology</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genetic Variation</topic><topic>Genotype</topic><topic>Haplotypes</topic><topic>Humans</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</topic><topic>MafF Transcription Factor - genetics</topic><topic>MAFG</topic><topic>MAFK</topic><topic>MafK Transcription Factor - genetics</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Nuclear Proteins - genetics</topic><topic>Odds Ratio</topic><topic>oxidative stress</topic><topic>Polymorphism, Single Nucleotide</topic><topic>polymorphisms</topic><topic>Proto-Oncogene Proteins c-maf - genetics</topic><topic>re-sequencing</topic><topic>Sex Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martínez-Hernández, Angelica</creatorcontrib><creatorcontrib>Gutierrez-Malacatt, Humberto</creatorcontrib><creatorcontrib>Carrillo-Sánchez, Karol</creatorcontrib><creatorcontrib>Saldaña-Alvarez, Yolanda</creatorcontrib><creatorcontrib>Rojas-Ochoa, Alberto</creatorcontrib><creatorcontrib>Crespo-Solis, Erick</creatorcontrib><creatorcontrib>Aguayo-González, Alvaro</creatorcontrib><creatorcontrib>Rosas-López, Adriana</creatorcontrib><creatorcontrib>Ayala-Sanchez, Jose Manuel</creatorcontrib><creatorcontrib>Aquino-Ortega, Xochitl</creatorcontrib><creatorcontrib>Orozco, Lorena</creatorcontrib><creatorcontrib>Cordova, Emilio J</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>European journal of haematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martínez-Hernández, Angelica</au><au>Gutierrez-Malacatt, Humberto</au><au>Carrillo-Sánchez, Karol</au><au>Saldaña-Alvarez, Yolanda</au><au>Rojas-Ochoa, Alberto</au><au>Crespo-Solis, Erick</au><au>Aguayo-González, Alvaro</au><au>Rosas-López, Adriana</au><au>Ayala-Sanchez, Jose Manuel</au><au>Aquino-Ortega, Xochitl</au><au>Orozco, Lorena</au><au>Cordova, Emilio J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Small MAF genes variants and chronic myeloid leukemia</atitle><jtitle>European journal of haematology</jtitle><addtitle>Eur J Haematol</addtitle><date>2014-01</date><risdate>2014</risdate><volume>92</volume><issue>1</issue><spage>35</spage><epage>41</epage><pages>35-41</pages><issn>0902-4441</issn><eissn>1600-0609</eissn><abstract>Chronic myeloid leukemia (CML) is one of the most frequent hematological neoplasia worldwide. The abnormal accumulation of reactive oxygen species may be an important factor in CML development. The transcription factor NRF2 can regulate the transcription of a battery of antioxidant and detoxificant genes after heterodimerizing with small‐Maf proteins. Although the participation of NRF2 in the development of chronic degenerative diseases has been thoroughly studied, the role of small‐Maf genes has not been documented. We have identified polymorphisms in the three MAF genes (F, G and K) and assessed their association with CML. Over 266 subjects with CML and 399 unrelated healthy donors have been studied. After sequencing each MAF gene by Sanger technology, we found 17 variants in MAFF gene, eight in MAFG and seven in MAFK. In the case‐control study, the homozygote genotype CC for the rs9610915 SNP of MAFF was significantly associated with CML. The frequency of the ACC haplotype from MAFK was significantly lower than controls. After stratification by gender, the ACC and GTG haplotypes were associated only with males with CML. These novel data suggest an association between MAFF and MAFG and the development of CML.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>24118457</pmid><doi>10.1111/ejh.12211</doi><tpages>7</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0902-4441
ispartof European journal of haematology, 2014-01, Vol.92 (1), p.35-41
issn 0902-4441
1600-0609
language eng
recordid cdi_proquest_miscellaneous_1534840101
source MEDLINE; Wiley Online Library Journals Frontfile Complete
subjects Adult
Alleles
Case-Control Studies
Computational Biology
Female
Gene Frequency
Genetic Variation
Genotype
Haplotypes
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
MafF Transcription Factor - genetics
MAFG
MAFK
MafK Transcription Factor - genetics
Male
Middle Aged
Nuclear Proteins - genetics
Odds Ratio
oxidative stress
Polymorphism, Single Nucleotide
polymorphisms
Proto-Oncogene Proteins c-maf - genetics
re-sequencing
Sex Factors
title Small MAF genes variants and chronic myeloid leukemia
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T21%3A23%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Small%20MAF%20genes%20variants%20and%20chronic%20myeloid%20leukemia&rft.jtitle=European%20journal%20of%20haematology&rft.au=Mart%C3%ADnez-Hern%C3%A1ndez,%20Angelica&rft.date=2014-01&rft.volume=92&rft.issue=1&rft.spage=35&rft.epage=41&rft.pages=35-41&rft.issn=0902-4441&rft.eissn=1600-0609&rft_id=info:doi/10.1111/ejh.12211&rft_dat=%3Cproquest_cross%3E1534840101%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1492700039&rft_id=info:pmid/24118457&rfr_iscdi=true